Cases reported "akinetic mutism"

Filter by keywords:

Retrieving documents. Please wait...

1/71. Reversible akinetic mutism possibly induced by baclofen.

    A 76-year-old man developed akinetic mutism after 3 days of receiving low-dosage baclofen. electroencephalography showed a diffusely slow background with intermittent generalized sharp wave discharges. The condition resolved after discontinuing baclofen. To our knowledge, this is the first reported case of baclofen-induced akinetic mutism in a patient with normal renal function. The pathophysiology of this condition is unknown, but it may result from selective binding of the drug to the gamma-aminobutyric acid-B receptors located in the frontal lobes or thalamic nuclei, interrupting the thalamocortical limbic pathways. ( info)

2/71. Aggravation of brainstem symptoms caused by a large superior cerebellar artery aneurysm after embolization by Guglielmi detachable coils--case report.

    An 81-year-old male presented with right oculomotor nerve paresis and left hemiparesis caused by a mass effect of a large superior cerebellar artery aneurysm. Endovascular treatment was performed using Guglielmi detachable coils. The patient subsequently suffered aggravation of the mass effect 3 weeks after the embolization. Bilateral vertebral artery occlusion was performed, which decreased the cerebral edema surrounding the aneurysm, but his neurological symptoms did not improve. Parent artery occlusion is recommended as the first choice of treatment for an unclippable large or giant aneurysm causing a mass effect on the brainstem. ( info)

3/71. Bilateral substantia nigra changes on MRI in a patient with encephalitis lethargica.

    A 33-year-old woman admitted for meningoencephalitis had features of encephalitis lethargica develop on her third day of illness. She had ophthalmoplegia, akinetic mutism, and prominent extrapyramidal signs consisting of lip and hand tremors, cogwheel rigidity, and facial bradykinesia. ( info)

4/71. neurologic manifestations of cerebral air embolism as a complication of central venous catheterization.

    OBJECTIVE, patients, AND methods: A severe case of cerebral air embolism after unintentional central venous catheter disconnection was the impetus for a systematic literature review (1975-1998) of the clinical features of 26 patients (including our patient) with cerebral air embolism resulting from central venous catheter complications. RESULTS: The jugular vein had been punctured in eight patients and the subclavian vein, in 12 patients. embolism occurred in four patients during insertion, in 14 patients during unintentional disconnection, and in eight patients after removal and other procedures. The total mortality rate was 23%. Two types of neurologic manifestations may be distinguished: group A (n = 14) presented with encephalopathic features leading to a high mortality rate (36%); and group B (n = 12) presented with focal cerebral lesions resulting in hemiparesis or hemianopia affecting mostly the right hemisphere, with a mortality rate as high as 8%. In 75% of patients, an early computed tomography indicated air bubbles, proving cerebral air embolism. Hyperbaric oxygen therapy was performed in only three patients (12%). A cardiac defect, such as a patent foramen ovale was considered the route of right to left shunting in 6 of 15 patients (40%). More often, a pulmonary shunt was assumed (9 of 15 patients; 60%). For the remainder, data were not available. CONCLUSION: When caring for critically ill patients needing central venous catheterization, nursing staff and physicians should be aware of this potentially lethal complication. ( info)

5/71. Total recovery after bilateral paramedian thalamic infarct.

    Bilateral paramedian thalamic infarcts are characterised initially by the association of acute vigilance disorders and vertical gaze palsy, followed by persisting dementia with severe mnemic disturbance, global aspontaneity and apathy. We describe a patient with a dramatic neuropsychological recovery, confirmed by testing examination and completed by a cerebral metabolism study. The pathophysiology of this type of cognitive deficit is discussed. ( info)

6/71. Reversible delayed leukoencephalopathy following intravenous heroin overdose.

    We present serial neuropsychological, magnetic resonance (MR) imaging and EEG changes in a case of widespread CNS myelinopathy due to intravenous heroin overdose complicated by a period of prolonged unconsciousness. Following recovery from the acute overdose, the subject had the delayed onset of akinetic mutism with urinary incontinence. Sequential formal neuro-psychological assessments over 9 months showed evolution from severe global cerebral dysfunction to moderate disturbance of frontal lobe function. Almost complete resolution of diffuse white matter signal changes, accompanied by the development of a degree of volume loss, was evident on serial MR imaging over the same period, and generalized arrhythmic delta-range slowing on the EEG evolved int o a near normal pattern. ( info)

7/71. Deep cerebral venous thrombosis: an illustrative case with reversible diencephalic dysfunction.

    BACKGROUND: Isolated thrombosis of the deep cerebral veins is rare and its diagnosis can be difficult. mortality is often high and little is known about the long-term prognosis. CASE REPORT: We report a 24-year-old woman with akinetic mutism and extensive bilateral thalamic lesions. CT and MRI allowed early diagnosis by demonstrating thrombosis within the internal cerebral veins, without the need for angiography. heparin treatment was used safely despite the presence of thalamic and intraventricular hemorrhage. After five weeks, the patient recovered rapidly and remains well at 18 months. Serial MRI showed dramatic resolution of the imaging abnormalities. CONCLUSIONS: The clinical features and characteristic neuroimaging appearance of deep cerebral venous thrombosis should be recognized by physicians caring for stroke patients. Deep cerebral venous thrombosis can produce extensive venous congestion and vasogenic edema without early infarction. Excellent clinical recovery is possible even after severe and prolonged neurological deficits. ( info)

8/71. BIPLEDs in akinetic mutism caused by bilateral anterior cerebral artery infarction.

    INTRODUCTION: akinetic mutism is described as a result of many disorders. Bilateral infarction of the anterior cerebral artery (ACA) territory is reported rarely, however, often leading to akinetic mutism. CASE REPORT: We report a 70 year-old man with akinetic mutism due to bilateral ACA infarction. electroencephalography, 24h after admission, showed bilateral independent periodic lateralized epileptiform discharges (BIPLEDs) in the frontal region and diffuse theta and polymorphic delta activity. DISCUSSION: Postanoxic encephalopathy, central nervous system infection and chronic seizure disorders are the major causes of BIPLEDs. However, BIPLEDs may occur in bilateral ACA territory infarction. ( info)

9/71. Recovery of children after severe head injury. Psychoreactive superimpositions.

    After the regaining of consciousness and awareness in the strange environment of an intensive care unit, an injured child is exposed to a situation of extreme psychological impact. This situation, in addition to a probably organically changed reactivity, is liable to provoke a particular, abnormal psychic response. The abnormal reaction can follow the pattern of a feigned-death response and thus mimic an organic coma vigile (apallic state). The resulting psychoreactive stuporous state ("Sleeping beauty syndrome") may lead to a misjudgement of the recovery degree and may delay early rehabilitation. With the help of a representative case, the clinical manifestation, course, and treatment of this reactive juvenile syndrome are presented. The interaction of physiogenic and psychogenic factors responsible for some psychiatric sequelae during the early period after head injury is emphasized. ( info)

10/71. Chronic akinetic mutism after mesencephalic-diencephalic infarction: remediated with dopaminergic medications.

    OBJECTIVE: akinetic mutism (AKM) is an uncommon disorder with a complex neuropathology. There is no generally accepted treatment, and it is not known if late treatments are effective. The relationship between AKM and abulia is uncertain. methods: The effects of dopaminergic treatment of a patient with chronic AKM after discrete bilateral infarctions of the mesencephalic ventral tegmental area and the lateral hypothalamus were studied with motor measures, the Functional Independence Measure (FIM), and neuropsychological tests. RESULTS: Treatment with a combination of carbidopa/levodopa and pergolide produced prompt amelioration of AKM with dramatic and rapid improvement in FIM. An apathetic, amotivational state persisted despite resolution of akinesia and normal frontal executive functions. CONCLUSIONS: AKM may respond to dopaminergic treatment even after months of severe akinesia. The mechanism of abulia is more complex than simply a partial dopaminergic deficiency state and may persist even when AKM is treated and frontal cognitive functions are normal. ( info)
| Next ->

Leave a message about 'Akinetic Mutism'

We do not evaluate or guarantee the accuracy of any content in this site. Click here for the full disclaimer.